We wished to evaluate the role of dynamic hyperinflation and dynamic airway compression as potential sources of exertional dyspnea in patients with chronic obstructive pulmonary disease (COPD). The rationale was that if such factors contribute importantly, then the administration of continuous positive airway pressure (CPAP), which serves to unload the inspiratory muscles and attenuate dynamic compression on expiration, should improve respiratory sensation. Further partitioning of CPAP into its continuous positive inspiratory pressure (CPIP) and continuous positive expiratory pressure (CPEP) components permitted an assessment of the relative importance of the above factors with respect to respiratory sensation. CPAP, CPIP, and CPEP (4 to 5 cm H2O each) were administered intermittently (for intervals of 40 to 60 s on each occasion) in random order during steady-state submaximal exercise in five patients with COPD (average FEV1, 40% predicted) and in five normal healthy subjects. Changes in the sense of breathing effort during the various pressure applications were assessed by asking the subjects to point to a category scale of -5 to +5, where -5 indicated that breathing was markedly easier and +5 indicated that breathing was markedly harder. CPAP, when administered to the COPD group, resulted in a highly significant (p less than 0.005) reduction in the sense of breathing effort. By contrast, CPAP significantly increased the sense of breathing effort in the normal group (p less than 0.01). CPIP facilitated breathing in both the COPD group and the normal group (p less than 0.05 and p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with severe COPD are frequently flow-limited during expiration at rest. When expiratory flow is at its maximum, application of negative pressure at the mouth should accentuate dynamic compression downstream from the flow-limiting segment (FLS) without substantially affecting flow or pressure upstream. The purpose of this study was to determine the ventilatory response to such intervention and to determine its effect on respiratory sensation. Such responses should reflect the effect of airway receptors downstream from the FLS. Nine patients with severe COPD (FEV, ± SE = 27 ± 3% predicted) breathed into a closed-circuit apparatus that incorporated a rolling-seal spirometer. The spirometer was fitted with a linear actuator that caused mouth pressure to become negative in proportion to expiratory flow (expiratory assistance, EA). Ventilatory responses were measured during 4 min of EA (-9.7 cm H20/L/s) and were compared with those during control periods (4 min each) before and after this (Ct and C2). Sense of breathing effort was assessed at 1-min intervals by asking the subject to point to a category scale of 1 to 5, with 1 being minimal effort and 5 indicating that breathing was very difficult. There were small but significant (p < 0.05) decreases in Ti (mean ± SE, -0.2 ± 0.05 s) and TE (-0.3 ± 0.07 s), with increases in breathing frequency (+2.25 ± 0.7) and ventilation (+1.5 ± 0.6 L/min). No significant changes were observed in tidal volume or end-expiratory volume. The EA caused a highly significant ( p < 0.001) increase in the sense of breathing effort. We conclude that dynamic compression of the airways caused a mild tachypnea and resulted in an unpleasant respiratory sensation. Such findings lend support to the hypothesis that upper airway mechanoreceptors actively modulate ventilatory control and may contribute to the sensation of dyspnea in patients with COPD. AM REV RESPIR DIS 1987; 135:912-918
To cope with the increased ventilatory demands of exercise, patients with severe expiratory flow limitation adopt strategies that ultimately place greater demands on their inspiratory muscles. Increased inspiratory muscle work may contribute to dyspnea causation and exercise limitation in such patients even before their ventilatory ceiling is attained. In this setting, continuous positive airway pressure (CPAP) should, by favorably affecting inspiratory muscle function and respiratory sensation, improve exercise performance. Six patients with chronic airflow limitation (CAL) (FEV1 +/- SD = 35 +/- 12% predicted) undertook constant-load, submaximal, cycle exercise at 50% of their predetermined maximal oxygen consumption: CPAP of 4 to 5 cm H2O was delivered during one exercise session and bracketed by one or two unassisted control sessions. In four patients, CPAP-assisted (4 to 5 cm H2O) exercise was bracketed by two unassisted control exercise sessions; two remaining patients undertook CPAP-assisted exercise and one unassisted control session. CPAP resulted in a significant increase in exercise endurance time (TLIM) (by 48%: CPAP TLIM (mean +/- SE) = 8.82 +/- 1.90 min; averaged control TLIM = 5.98 +/- 1.23 min (p less than 0.01). CPAP effectively ameliorated exertional dyspnea in the majority of patients; selected dyspnea ratings (Borg scale) during control (final minute) and CPAP at isotime, at comparable levels of ventilation, were (mean +/- SD) 7.83 +/- 2.25 and 5.5 +/- 2.2, respectively (p less than 0.025). Breathing frequency fell significantly during CPAP application (at isotime) by 17% (p less than 0.02); other steady-state ventilatory variables and end-expiratory lung volumes were not significantly different during CPAP and control.(ABSTRACT TRUNCATED AT 250 WORDS)
The alterations in lung function and breathing pattern were examined in 6 quadriplegics at 3, 6 and greater than 12 months post injury, and were compared to 6 able bodied controls. Subjects were studied in both the seated and supine positions. Functional residual capacity (FRC), forced vital capacity (FVC), inspiratory capacity (IC), and maximum mouth pressure (Pimax) at FRC were measured. Total lung capacity (TLC) and residual volume (RV) were calculated. Resting breathing pattern was assessed for 20 minutes from a spirogram derived from summed rib cage and abdominal strain gauge signals. At 3 months in quadriplegics, TLC was reduced (p less than 0.05), RV increased (p less than 0.01) and FRC was normal in sitting; in supine, only TLC was reduced (p less than 0.05); Pimax was decreased (p less than 0.01) in both positions in quadriplegics at 3 months, but increased over the first year in the seated position (p less than 0.01). There were no alterations in breathing pattern at any time interval in quadriplegics in supine. In contrast, at 3 months post injury in sitting, expiratory time (Te) was shortened (p less than 0.05), tidal volume (Vt) was decreased, and heart rate elevated as compared to controls (p less than 0.05). Inspiratory time (Ti) was not significantly shortened at 3 months in quadriplegics, but a lengthening of Ti occurred between 3 and 6 months (p less than 0.025) resulting in increased Vt, and heart rate decreased to normal. Vt/Ti was reduced, and did not alter with time. The lengthening of Ti/Ttot observed in supine in control subjects (p less than 0.025), was not observed in quadriplegics. Quadriplegics sighed as frequently in supine as did controls at all stages post injury, whereas they decreased sighing frequency in sitting at 3 and 6 months post injury (p less than 0.05). The improvement in resting breathing pattern observed in quadriplegics in sitting with time, may be due to increased accessory muscle function, improved chest wall stability and thoracoabdominal coupling, or a combination of these factors. It is also possible that the alterations in breathing pattern were a response to cardiovascular adjustments occurring in the same time frame. Quadriplegics retain the sigh reflex, but do not take as many big breaths in sitting as they do in supine, probably due to the increased work of breathing in the seated posture.
To determine whether upper airway mechanoreceptors partly subserve the ventilatory response to external mechanical loading in conscious humans, we studied 11 laryngectomized subjects. The oropharynx (OP) or tracheostomy was selectively loaded (in random order) by attaching the mouth or tracheal tube to a special pressure-generating apparatus, and steady-state ventilatory responses were recorded. Phasic negative pressure changes generated at the OP to simulate inspiratory resistive loading, expiratory resistive unloading, and elastic loading resulted in trivial prolongation of inspiratory duration by 12, 9, and 4%, respectively; other ventilatory variables were not significantly altered. Phasic positive pressure changes at the OP that simulated inspiratory resistive unloading and expiratory resistive loading had little effect on breathing pattern. When the above loads were applied via the tracheostomy, using pressures of similar magnitude, ventilatory responses were qualitatively similar and quantitatively not significantly different from those of normal healthy controls. The results suggest that the OP does not make an important contribution to ventilatory responses during external mechanical loading in conscious humans. Loading responses to conventional mechanical loads are preserved in the absence of afferent information from the upper airways.
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